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Markers of blood coagulation and fibrinolysis in patients with early and delayed microsurgical reconstructions in the lower extremities.
Journal of Plastic Surgery and Hand Surgery 2017 December
BACKGROUND: In this study, markers of coagulation and fibrinolysis were assessed during early and delayed microsurgical reconstruction in patients with traumatic defects of their lower legs to analyse whether an imbalance of the hemostasis after trauma might predispose the development of vascular complications.
METHODS: The prospective study included 70 patients. In 35 patients, surgery was performed within 72 hours after injury. In 35 other patients, delayed free flap transfer was performed between 14-21 days after trauma. In each group, reconstruction was performed with a fasciocutaneous anterior-lateral thigh flap (ALT, n = 18) or a myocutaneous flap (latissimus dorsi flap; n = 17). Blood samples were collected preoperatively, intraoperatively, and 3, 6, 12, 24, 36, 48, 72, 96 and 120 hours after the operation. Analysed parameters included markers of coagulation such as prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III-complex (TAT), and antithrombin, as well as fibrinolysis markers such as plasminogenactivator inhibitor-I (PAI-1), tissue-plasminogenactivator (t-PA), and plasminogen.
RESULTS: Preoperatively, levels of F1 + 2, TAT, and PAI-1 were significantly higher in patients with delayed reconstruction (p < .05). Patients with later vascular complications in this group (n = 5) presented a significant higher concentration of TAT, F1 + 2, and PAI-1 (p < .05). Twelve and 24 hours after free flap surgery, patients with vascular complications presented significant elevated levels of these markers (p < .05).
CONCLUSIONS: Patients with delayed free flap surgery after lower leg trauma present a hypercoagulable state in their blood due to activation of the coagulation system and hypofibrinolysis. Early reconstruction might minimise the risk of flap failure caused by hypercoagulability.
METHODS: The prospective study included 70 patients. In 35 patients, surgery was performed within 72 hours after injury. In 35 other patients, delayed free flap transfer was performed between 14-21 days after trauma. In each group, reconstruction was performed with a fasciocutaneous anterior-lateral thigh flap (ALT, n = 18) or a myocutaneous flap (latissimus dorsi flap; n = 17). Blood samples were collected preoperatively, intraoperatively, and 3, 6, 12, 24, 36, 48, 72, 96 and 120 hours after the operation. Analysed parameters included markers of coagulation such as prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III-complex (TAT), and antithrombin, as well as fibrinolysis markers such as plasminogenactivator inhibitor-I (PAI-1), tissue-plasminogenactivator (t-PA), and plasminogen.
RESULTS: Preoperatively, levels of F1 + 2, TAT, and PAI-1 were significantly higher in patients with delayed reconstruction (p < .05). Patients with later vascular complications in this group (n = 5) presented a significant higher concentration of TAT, F1 + 2, and PAI-1 (p < .05). Twelve and 24 hours after free flap surgery, patients with vascular complications presented significant elevated levels of these markers (p < .05).
CONCLUSIONS: Patients with delayed free flap surgery after lower leg trauma present a hypercoagulable state in their blood due to activation of the coagulation system and hypofibrinolysis. Early reconstruction might minimise the risk of flap failure caused by hypercoagulability.
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